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Published on: December 16, 2015
Maternal adiponectin controls milk composition to prevent neonatal inflammation
Zixue Jin1, Yang Du, Adam G Schwaid
1Department of Pharmacology (Z.J., Y.D., Y.W.), Touchstone Diabetes Center and Department of Internal Medicine (I.W.A., P.E.S.), The University of Texas Southwestern Medical Center, Dallas, Texas 75390; and Department of Chemistry and Chemical Biology (A.G.S., A.S.), Harvard University, Cambridge, Massachusetts 02138.
Maternal adiponectin levels critically influence infant inflammation during lactation. Both too much and too little adiponectin cause inflammation in pups, which can be treated by inhibiting Toll-like receptor 2/4 (TLR2/4).
Area of Science:
- Endocrinology
- Immunology
- Developmental Biology
Background:
- Adiponectin, an adipokine, is linked to metabolic and inflammatory disorders.
- Its role in lactation and infant health is largely unknown.
Purpose of the Study:
- To investigate the function of maternal adiponectin in regulating neonatal inflammatory status during lactation.
- To elucidate the mechanisms by which adiponectin influences milk composition and infant inflammation.
Main Methods:
- Utilized transgenic and knockout mouse models with altered maternal adiponectin levels.
- Analyzed mammary gland inflammation, milk composition (fatty acids), and neonatal systemic inflammation (alopecia).
- Investigated the role of Toll-like receptor (TLR) 2/4 signaling in mediating adiponectin-induced inflammation in neonates.
Main Results:
- Both maternal adiponectin deficiency and overexpression led to systemic inflammation and alopecia in nursing pups.
- Adiponectin deficiency increased mammary gland leukocyte infiltration and inflammatory cytokines.
- Adiponectin overabundance resulted in increased milk lipid accumulation and excessive saturated fatty acids.
- Inflammation and alopecia in pups were rescued in Toll-like receptor (TLR) 2/4 double-knockout pups.
- Long-chain saturated fatty acids activate inflammatory genes via TLR2/4, potentiated by cytokines.
Conclusions:
- Adiponectin is a dosage-dependent regulator of lactation and milk quality, impacting neonatal inflammation.
- Maternal adiponectin dysregulation can cause infantile inflammatory disorders.
- Toll-like receptor (TLR) 2/4 inhibition presents a potential therapeutic strategy for these conditions.
